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    Saikosaponin A
    CAS No. 20736-09-8 Price $80 / 20mg
    Catalog No.CFN99987Purity>=98%
    Molecular Weight780.99Type of CompoundTriterpenoids
    FormulaC42H68O13Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Size /Price /Stock 10 mM * 1 mL in DMSO / $44.7 / In-stock
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  • Biological Activity
    Description: Saikosaponin A has a variety of pharmacological benefits, including antiepileptic, anti-osteoporosis, antioxidant, anti-inflammatory, immunomodulatory, and anti-bacterial activities. It extends to alcohol self-administration the capacity to suppress morphine and cocaine self-administration in rats, and can effectively attenuate neuropathic pain in CCI rats by inhibiting the activation of p38 MAPK and NF-κB signaling pathways in spinal cord. It can inhibit NMDA receptor current and persistent sodium current, and inhibit the TNF-α level, the IL-1β production, and cysteine-aspartic acid protease (caspase)-1 activity.
    Targets: COX | NOS | TNF-α | IL Receptor | NF-kB | p65 | p38MAPK | JNK | ERK | GABA Receptor | Caspase | Potassium Channel | IkB | IKK
    In vitro:
    Int Immunopharmacol. 2015 Mar;25(1):49-54.
    Saikosaponin a inhibits RANKL-induced osteoclastogenesis by suppressing NF-κB and MAPK pathways.[Pubmed: 25617149]
    Inflammatory cytokines play an important role in osteoclastogenesis. Saikosaponin A (SSa) possesses anti-inflammatory activity. However, the role of SSa in osteoporosis is still unclear. Therefore, the objective of this study was to investigate the effects of SSa on receptor activator of the nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis and signaling pathway by in vitro assay.
    In mouse bone marrow monocytes (BMMs), SSa suppressed RANKL plus macrophage colony-stimulating factor (M-CSF)-induced osteoclast differentiation in a dose-dependent manner. Moreover, SSa decreased osteoclastogenesis-related marker proteins expression, including NFATc1, c-fos and cathepsin K. At molecular levels, SSa inhibited RANKL-induced IκBα phosphorylation, p65 phosphorylation and NF-κB luciferase activity in RAW264.7 cells. And SSa also suppressed RANKL-induced p-38, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) phosphorylation.
    Taken together, these findings suggest that SSa suppresses osteoclastogenesis through inhibiting RANKL-induced p-38, ERK, JNK and NF-κB activation. SSa is a novel agent in the treatment of osteoclast-related diseases, such as osteoporosis.
    Evid Based Complement Alternat Med. 2013;2013:413092.
    Saikosaponin a Enhances Transient Inactivating Potassium Current in Rat Hippocampal CA1 Neurons.[Pubmed: 23554830 ]
    Saikosaponin A (SSa), a main constituent of the Chinese herb Bupleurum chinense DC., has been demonstrated to have antiepileptic activity. Recent studies have shown that SSa could inhibit NMDA receptor current and persistent sodium current. However, the effects of SSa on potassium (K(+)) currents remain unclear. In this study, we tested the effect of SSa on 4AP-induced epileptiform discharges and K(+) currents in CA1 neurons of rat hippocampal slices.
    We found that SSa significantly inhibited epileptiform discharges frequency and duration in hippocampal CA1 neurons in the 4AP seizure model in a dose-dependent manner with an IC 50 of 0.7  μ M. SSa effectively increased the amplitude of I Total and I A , significantly negative-shifted the activation curve, and positive-shifted steady-state curve of I A . However, SSa induced no significant changes in the amplitude and activation curve of I K . In addition, SSa significantly increased the amplitude of 4AP-sensitive K(+) current, while there was no significant change in the amplitude of TEA-sensitive K(+) current.
    Together, our data indicate that SSa inhibits epileptiform discharges induced by 4AP in a dose-dependent manner and that SSa exerts selectively enhancing effects on I A . These increases in I A may contribute to the anticonvulsant mechanisms of SSa.
    In vivo:
    Neurosci Lett. 2016 May 16;621:62-67.
    Reducing effect of saikosaponin A, an active ingredient of Bupleurum falcatum, on alcohol self-administration in rats: Possible involvement of the GABAB receptor.[Pubmed: 27080427 ]
    Recent studies demonstrated that treatment with Saikosaponin A (SSA) - an active ingredient of the medicinal herb, Bupleurum falcatum L. - selectively suppressed, likely via a GABAB receptor-mediated mechanism, intravenous self-administration of morphine and cocaine in rats [Yoon et al., 2012; 2013]. The present study was designed to investigate whether the capacity of SSA to suppress morphine and cocaine self-administration extends to oral alcohol self-administration.
    To this end, selectively bred Sardinian alcohol-preferring (sP) rats were trained to lever-respond on a Fixed Ratio (FR) 4 (FR4) schedule of reinforcement for alcohol (15%, v/v) in daily 30-min sessions. Once responding had stabilized, rats were tested under the FR4 (measure of alcohol reinforcing properties) and Progressive Ratio (PR; measure of alcohol motivational properties) schedules of reinforcement. The possible involvement of the GABAB receptor system was investigated testing the effect of (a) pretreatment with the GABAB receptor antagonist, SCH50911, and (b) combined treatment with the positive allosteric modulator of the GABAB receptor, GS39783. Treatment with SSA (0, 0.25, 0.5, and 1mg/kg, i.p.) markedly reduced lever-responding for alcohol, amount of self-administered alcohol, and breakpoint for alcohol (defined as the lowest response requirement not achieved in the PR experiment). Pretreatment with 2mg/kg SCH50911 (i.p.) resulted in a partial blockade of the reducing effect of 0.5mg/kg SSA on lever-responding for alcohol and amount of self-administered alcohol. Combination of per se ineffective doses of GS39783 (5mg/kg, i.g.) and SSA (0.1mg/kg, i.p.) reduced lever-responding for alcohol and amount of self-administered alcohol.
    These results (a) extend to alcohol self-administration the capacity of SSA to suppress morphine and cocaine self-administration in rats and (b) suggest that the GABAB receptor system is likely part of the neural substrate underlying the reducing effect of SSA on alcohol self-administration.
    Am. J. Chinese Med., 2012, 38(1):99-111.
    Curcumin and Saikosaponin A Inhibit Chemical-Induced Liver Inflammation and Fibrosis in Rats[Pubmed: 20128048]
    Curcumin and Saikosaponin A as antioxidants improve antioxidant status. This study investigated the anti-inflammatory and antifibrotic actions of curcumin and Saikosaponin A on CCl(4)-induced liver damage.
    Sprague-Dawley rats were randomly divided into control, CCl(4), CCl(4)+ curcumin (0.005%; CU), CCl(4) + Saikosaponin A (0.004%; SS), and CCl(4) + curcumin + Saikosaponin A (0.005% + 0.004%; CU + SS) groups. Carbon tetrachloride (40% in olive oil) at a dose of 0.75 ml/kg was injected intraperitoneally once a week. Curcumin and Saikosaponin A were supplemented alone or in combination with diet 1 week before CCl(4) injection for 8 weeks. After 8-week supplementation, histopathological results showed hepatic collagen deposition was significantly reduced in the CU and SS groups, and activated nuclear factor-kappa B expression induced by CCl(4) in the liver was significantly inhibited by curcumin and/or Saikosaponin A. Hepatic proinflammatory cytokines tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 were significantly inhibited, and anti-inflammatory cytokine interleukin-10 was significantly increased by supplementation with curcumin and/or Saikosaponin A. Additionally, curcumin and/or Saikosaponin A significantly reduced the increased levels of hepatic transforming growth factor-beta1 and hydroxyproline after CCl(4) treatment.
    Therefore, supplementation with curcumin and/or Saikosaponin A suppress inflammation and fibrogenesis in rats with CCl(4)-induced liver injury. However, the combination has no additive effects on anti-inflammation and antifibrosis.
    Saikosaponin A Description
    Source: The roots of Bupleurum chinense DC.
    Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.2804 mL 6.4021 mL 12.8043 mL 25.6085 mL 32.0107 mL
    5 mM 0.2561 mL 1.2804 mL 2.5609 mL 5.1217 mL 6.4021 mL
    10 mM 0.128 mL 0.6402 mL 1.2804 mL 2.5609 mL 3.2011 mL
    50 mM 0.0256 mL 0.128 mL 0.2561 mL 0.5122 mL 0.6402 mL
    100 mM 0.0128 mL 0.064 mL 0.128 mL 0.2561 mL 0.3201 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Cell Research:
    Exp Ther Med. 2013 May;5(5):1345-1350.
    Saikosaponin A mediates the inflammatory response by inhibiting the MAPK and NF-κB pathways in LPS-stimulated RAW 264.7 cells.[Pubmed: 23737876]
    Saikosaponin A (SSA) is a major triterpenoid saponin isolated from Radix bupleuri (RB), a widely used Chinese traditional medicine to treat various inflammation-related diseases. The aim of this study was to investigate the anti-inflammatory activity, as well as the molecular mechanism of SSA in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells.
    In this study, we demonstrated that SSA markedly inhibits the expression of certain immune-related cytotoxic factors, including cyclooxygenase-2 (COX-2) and inducible nitric-oxide synthase (iNOS), as well as pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6. It also significantly upregulates the expression of IL-10, an important anti-inflammatory cytokine, suggesting its anti-inflammatory activity in LPS-stimulated macrophages. We further demonstrated that SSA inhibits the activation of the nuclear factor-κB (NF-κB) signaling pathway by suppressing the phosphorylation of inhibitory NF-κB inhibitor α (IκBα) and thus holding p65 NF-κB in the cytoplasm to prevent its translocation to the nucleus. In addition, SSA also inhibits the mitogen-activated protein kinase (MAPK) signaling pathway by downregulating the phosphorylation of p38 MAPK, c-Jun N-terminal kinase (c-JNK) and extracellular signal-regulated kinase (ERK), the three key components of the MAPK family.
    In conclusion, our study demonstrates that SSA has an anti-inflammatory effect by regulating inflammatory mediators and suppressing the MAPK and NF-κB signaling pathways in LPS-stimulated RAW 264.7 cells.
    Animal Research:
    Neurochem Res. 2014 Nov;39(11):2136-42.
    Attenuation of neuropathic pain by saikosaponin a in a rat model of chronic constriction injury.[Pubmed: 25107300]
    Despite immense advances in the treatment strategies, the effective treatment of patients suffering from neuropathic pain remains challenging. Saikosaponin A possesses anti-inflammatory activity. However, the role of Saikosaponin A in neuropathic pain is still unclear. Therefore, the objective of this study was to investigate the effects of Saikosaponin A on neuropathic pain.
    Neuropathic pain was induced by chronic constriction injury (CCI) of the sciatic nerve in rats. After CCI, rats were administered Saikosaponin A (6.25, 12.50 and 25.00 mg/kg intraperitoneal, once daily) for 14 days. Mechanical withdrawal threshold and thermal withdrawal latency were assessed before surgery and on days 1, 3, 7, and 14 after CCI. Our results showed that CCI significantly decreased mechanical withdrawal threshold and thermal withdrawal latency on days 1, 3, 7 and 14, as compared with sham groups, however, Saikosaponin A reversed this effects. In addition, Saikosaponin A inhibited CCI-induced the levels of TNF-α, IL-1β, IL-2 in spinal cord. Western blot analysis demonstrated that Saikosaponin A reduced the elevated expression of p-p38 mitogen-activated protein kinase (MAPK) and NF-κB in the spinal cord induced by CCI.
    These results suggest that Saikosaponin A could effectively attenuate neuropathic pain in CCI rats by inhibiting the activation of p38 MAPK and NF-κB signaling pathways in spinal cord.
    Biol. Pharm. Bull., 2011, 34(6):817-23.
    Inactivation of cystein-aspartic acid protease (caspase)-1 by saikosaponin A.[Pubmed: 21628878]
    This work investigates the anti-inflammatory mechanism of Saikosaponin A (SA), a major component of Bupleurum falcatum LINNE.
    SA significantly inhibited phorbol myristate acetate (PMA) plus A23187-induced the production and expression of interleukin (IL)-6 and tumor necrosis factor (TNF)-α in human mast cell (HMC)-1 cells. SA suppressed PMA plus A23187-induced phosphorylation of extracellular signal-regulated kinase and p38. When HMC-1 cells were treated with SA, translocation of nuclear factor (NF)-κB/Rel A into nucleus and degradation of inhibitor of NF-κB (IκB) in cytoplasm were inhibited. SA decreased PMA plus A23187-induced cysteine-aspartic acid protease (caspase)-1 activity. IL-1β production was also inhibited by SA. Finally, SA significantly decreased the number of nasal rubs and serum TNF-α level in the ovalbumin-sensitized allergic rhinitis mouse model.
    The underlying mechanism involves, at least in part, inactivation of caspase-1, which provides new evidence for therapeutic application of SA to target inflammatory processes.